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H. pylori infection is related to mitochondrial microsatellite instability in gastric carcinogenesis.

Ling X, Zhang H, Shen C, Yan W, Wang P, Feng J, Peng Z, Peng G, Chen W, Fang D - Infect. Agents Cancer (2016)

Bottom Line: The levels of IL-8 were significantly higher in specimens with mtMSI than in those without mtMSI (P < 0.01).An association of mtMSI with the intestinal histological type was found (P < 0.05).Increased IL-8 levels induced by H. pylori were related to the invasion, lymphnode spreading and clinical stage of gastric cancer (P < 0.05).Our results support a role for mtMSI in different mechanisms of gastric carcinogenesis.

View Article: PubMed Central - PubMed

Affiliation: Department of Gastroenterology, Southwest Hospital, Third Military Medical University, Chongqing, 400038 China.

ABSTRACT

Bachground: To assess the correlation of H. pylori infection with mitochondrial microsatellite instability (mtMSI) and IL-8 in gastric carcinogenesis.

Methods: H. pylori infection was evaluated through histology and a urease breath test; mtMSI was measured using PCR-single strand conformation polymorphism (PCR-SSCP); IL-8 was analyzed with ELISA methods.

Results: The detection rate of mtMSI was significantly higher in specimens with H. pylori infection than in those without H. pylori infection (P < 0.05). The levels of IL-8 were significantly higher in specimens with mtMSI than in those without mtMSI (P < 0.01).An association of mtMSI with the intestinal histological type was found (P < 0.05). Increased IL-8 levels induced by H. pylori were related to the invasion, lymphnode spreading and clinical stage of gastric cancer (P < 0.05).

Conclusions: H. pylori infection is related to mitochondrial microsatellite instability in the early steps of gastric cancer development. IL-8 may play a role in the development of mtMSI induced by H. pylori. Our results support a role for mtMSI in different mechanisms of gastric carcinogenesis.

No MeSH data available.


Related in: MedlinePlus

IL-8 levels in gastric mucosae with mtMSI. The levels of IL-8 were significantly higher in gastric mucosae with mtMSI than in those without mtMSI (*P < 0.05)
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Fig3: IL-8 levels in gastric mucosae with mtMSI. The levels of IL-8 were significantly higher in gastric mucosae with mtMSI than in those without mtMSI (*P < 0.05)

Mentions: The relationship between IL-8 expression and mtMSI is shown in Fig. 3. The levels of IL-8 were significantly higher in gastric mucosae with mtMSI than in those without mtMSI (P < 0.05).Fig. 3


H. pylori infection is related to mitochondrial microsatellite instability in gastric carcinogenesis.

Ling X, Zhang H, Shen C, Yan W, Wang P, Feng J, Peng Z, Peng G, Chen W, Fang D - Infect. Agents Cancer (2016)

IL-8 levels in gastric mucosae with mtMSI. The levels of IL-8 were significantly higher in gastric mucosae with mtMSI than in those without mtMSI (*P < 0.05)
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4940710&req=5

Fig3: IL-8 levels in gastric mucosae with mtMSI. The levels of IL-8 were significantly higher in gastric mucosae with mtMSI than in those without mtMSI (*P < 0.05)
Mentions: The relationship between IL-8 expression and mtMSI is shown in Fig. 3. The levels of IL-8 were significantly higher in gastric mucosae with mtMSI than in those without mtMSI (P < 0.05).Fig. 3

Bottom Line: The levels of IL-8 were significantly higher in specimens with mtMSI than in those without mtMSI (P < 0.01).An association of mtMSI with the intestinal histological type was found (P < 0.05).Increased IL-8 levels induced by H. pylori were related to the invasion, lymphnode spreading and clinical stage of gastric cancer (P < 0.05).Our results support a role for mtMSI in different mechanisms of gastric carcinogenesis.

View Article: PubMed Central - PubMed

Affiliation: Department of Gastroenterology, Southwest Hospital, Third Military Medical University, Chongqing, 400038 China.

ABSTRACT

Bachground: To assess the correlation of H. pylori infection with mitochondrial microsatellite instability (mtMSI) and IL-8 in gastric carcinogenesis.

Methods: H. pylori infection was evaluated through histology and a urease breath test; mtMSI was measured using PCR-single strand conformation polymorphism (PCR-SSCP); IL-8 was analyzed with ELISA methods.

Results: The detection rate of mtMSI was significantly higher in specimens with H. pylori infection than in those without H. pylori infection (P < 0.05). The levels of IL-8 were significantly higher in specimens with mtMSI than in those without mtMSI (P < 0.01).An association of mtMSI with the intestinal histological type was found (P < 0.05). Increased IL-8 levels induced by H. pylori were related to the invasion, lymphnode spreading and clinical stage of gastric cancer (P < 0.05).

Conclusions: H. pylori infection is related to mitochondrial microsatellite instability in the early steps of gastric cancer development. IL-8 may play a role in the development of mtMSI induced by H. pylori. Our results support a role for mtMSI in different mechanisms of gastric carcinogenesis.

No MeSH data available.


Related in: MedlinePlus